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Biomedical subjects

O Larsson

Publications and source records attributed to O Larsson.

At least 163 records · Page 9Linked to original sources
PubMed1989

The effects of tunicamycin, mevinolin and mevalonic acid on HMG-CoA reductase activity and nuclear division in the myxomycete Physarum polycephalum.

The effects of two inhibitors of 3-hydroxy 3-methyl glutaryl-coenzyme A reductase (tunicamycin and mevinolin) on nuclear division in the myxomycete Physarum polycephalum were examined. Tunicamycin exerted a minor effect on division in synchronized cultures, whereas mevinolin delayed the second, third and fourth nuclear divisions with increasing efficiency. Mevinolin also appeared to be the more potent inhibitor of HMG-CoA reductase, which catalyses the rate-limiting step in the biosynthesis of cholesterol and other isoprene derivatives. These effects of mevinolin could be partially reversed by the addition of mevalonate, suggesting that mevinolin exerts its inhibitory effects on Physarum nuclear division by decreasing the activity of HMG-CoA reductase.

Cell Nucleus↗
PubMed1988

Neuropeptide Y receptor in pig spleen: binding characteristics, reduction of cyclic AMP formation and calcium antagonist inhibition of vasoconstriction.

Specific, high-affinity binding sites for 125I-porcine neuropeptide Y (NPY) were demonstrated in membranes from the pig spleen. The equilibrium dissociation constant (KD) of the receptor 125I-NPY complex was 532 +/- 87 pM and the maximal number of specific binding sites (Bmax) 23 +/- 3 fmol/mg protein. The Scatchard plot for 125I-NPY binding under equilibrium conditions showed a best-fit to a straight line, whereas the dissociation appeared biphasic. 125I-NPY binding was unaffected by adrenoceptor antagonists and was inhibited by the guanosine triphosphate (GTP) analogue guanylylimidodiphosphate, suggesting regulation by a GTP binding protein. A series of NPY analogues showed a good correlation between binding, inhibition of forskolin-induced cyclic adenosine monophosphate (cAMP) formation and vasoconstrictor activity in vivo. A large carboxyl terminal portion of NPY and the carboxyl terminal amide were essential for binding, inhibition of cAMP formation and vasoconstrictor effects. The NPY fragment 13-36, which has been reported to act only on prejunctional NPY receptors, showed only a 10-fold lower potency than NPY-(1-36) both in binding to splenic membranes and vasoconstrictor activity in vivo. Phenylephrine increased phosphatidyl inositol turnover whereas NPY-(1-36) or -(13-36) did not induce formation of inositol phosphates. The calcium antagonists felodipine and nifedipine attenuated the splenic vasoconstrictor response to NPY in vivo but not the NPY-evoked inhibition of cAMP accumulation or the specific binding of 125I-NPY.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Neuropeptide Y- and alpha-adrenergic receptors in pig spleen: localization, binding characteristics, cyclic AMP effects and functional responses in control and denervated animals.

The localization of neuropeptide Y binding sites in the pig spleen, as revealed by [125I]Bolton-Hunter-labelled porcine neuropeptide Y and alpha 1-adrenergic receptor binding sites, as revealed by [125I](2-beta/4-hydroxy-phenyl/-ethylaminomethyl)-tetralone as radioligand, was compared with the distribution of neuropeptide Y and noradrenaline nerves, the latter revealed by tyrosine hydroxylase and dopamine-beta-hydroxylase, using immunohistochemistry. A large degree of codistribution was obtained between [125I]neuropeptide Y and alpha 1-binding sites in the capsule, trabeculae, blood vessels and the red pulp of the spleen. Neuropeptide Y and tyrosine hydroxylase as well as dopamine-beta-hydroxylase-positive nerves were identical in the spleen and had a similar gross distribution pattern as the [125I]neuropeptide Y and alpha 1 binding sites. In functional studies using the isolated blood-perfused spleen from pentobarbital-anaesthetized pigs, neuropeptide Y, noradrenaline and the alpha 1-selective agonist phenylephrine contracted the capsule and induced vasoconstriction in the spleen in vivo. However, the selective alpha 2-adrenoceptor agonists clonidine and azepexole had no effects on blood flow or perfusion pressure, suggesting that postjunctional alpha-receptors were of the alpha 1 type. Neuropeptide Y inhibited the forskolin-evoked, cyclic adenosine monophosphate formation in vitro. The [125I]neuropeptide Y binding, with an equilibrium-dissociation constant of 503 +/- 73 pM and a maximal number of specific binding sites of 23 +/- 3 fmol/mg protein, the neuropeptide Y-induced perfusion-pressure increase in vivo and the inhibition of forskolin-evoked cyclic adenosine monophosphate formation in vitro were dependent on the amidation of the C-terminal portion of the peptide molecule. Furthermore, the effects of neuropeptide Y were not changed by alpha- and beta-adrenoceptor blockade using prazosin and propranolol. Two weeks after postganglionic denervation the neuropeptide Y and the noradrenaline contents of the pig spleen were reduced by 97% and 99%, respectively. These changes were associated with a selective supersensitivity for the noradrenaline-induced perfusion-pressure increase in vivo compared with the effect of neuropeptide Y. However, a similar potentiation of the noradrenaline effect was induced by the monoamine-uptake blocker desipramine in the absence of denervation, and there was no change in the functional response to phenylephrine after denervation.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1988

The effects of glycosylation inhibitors on the proliferation of a spontaneously transformed cell line (3T6) in vitro.

We have examined the effects of different inhibitors of glycosylation processing on the proliferation of a spontaneously transformed murine cell line (3T6) in vitro. It was found that whereas two compounds that specifically inhibit distal steps in the glycosylation chain (swainsonine and castanospermine) only exerted marginal inhibitory effects on cell multiplication, a proximal inhibitor (tunicamycin) efficiently decreased the rate of DNA synthesis in a dose-dependent fashion. This tunicamycin-induced inhibitory effect on cell proliferation was cell cycle-specific, in the sense that cells in G1 only were blocked in their cell cycle progression. Like others (Volpe & Goldberg, 1983), we found that tunicamycin inhibited the activity of 3-hydroxy-3-methylglutaryl coenzyme-A reductase (HMG-CoA), which constitutes the ratelimiting step in the biosynthesis of cholesterol and isoprenoid derivatives, by catalysing the reduction of HMG-CoA to mevalonate, and it has been suggested that it plays a role in the control of cell proliferation and in tumour transformation. This raises the question as to whether tunicamycin exerts its inhibitory effects on cell proliferation via the isprene-synthetic pathway in addition to its effects on aspargine-linked glycosylation. By adding exogenous mevalonate, the rate-limiting step at which HMG-CoA reductase converts HMG-CoA to mevalonate can be bypassed. We found that addition of mevalonate partially reverses the effects of tunicamycin on cell proliferation. This suggests that tunicamycin exerts different effects, which taken together lead to a cessation of cell proliferation. One of these effects is likely to be mediated via the mevalonate-synthetic pathway.

Alkaloids↗
PubMed1988

The role of HMG CoA reductase and dolichol synthesis in the control of 3T6 cell proliferation: effects of cell crowding, serum depletion and addition of epidermal growth factor.

The proliferation of 3T6 cells was substantially decreased when the monolayer cultures were allowed to reach confluency. This growth inhibition (so-called density-dependent inhibition) was of the same magnitude as that following serum depletion in non-confluent cultures. Each type of growth inhibition was correlated to a depression of the activity of 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG CoA) reductase, an enzyme that regulates the biosynthesis of cholesterol and isoprenoid derivatives (e.g. dolichol) by catalysing the reduction of HMG CoA (which is derived from acetyl-CoA) into mevalonate. However, the depression of enzyme activity was more substantial in cells exposed to cell crowding than that in serum-depleted cells (87 and 48%, respectively). On the other hand, there was a 60-65% inhibition of the incorporation of mevalonate into dolichol due to serum deprivation, while it remained at normal level in confluent cultures, which implies that the inhibitory effects on dolichol synthesis due to these two experimental conditions were approximately equipotent. Addition of epidermal growth factor (EGF) to the cell cultures, whose proliferation was inhibited due to serum depletion, restored DNA synthesis completely, and these effects were related to a normalization of the activity of HMG CoA reductase and of the incorporation of mevalonate into dolichol. In contrast, in confluent cells addition of EGF only caused a slight increase in DNA synthesis and activity of HMG CoA reductase, and there was no significant increase in the incorporation of mevalonate into dolichol either.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Mevalonic acid products as mediators of cell proliferation in simian virus 40-transformed 3T3 cells.

Effects of treatment with serum-free medium and 25-hydroxycholesterol (25-OH) on the cell cycle of simian virus 40-transformed 3T3 fibroblasts, designated SV-3T3 cells, were studied and compared with simultaneous effects on the activity of 3-hydroxy-3-methylglutaryl (HMG) CoA reductase and incorporation of [3H]mevalonic acid into cholesterol, Coenzyme Q, and dolichol. The data confirm our previous finding (O. Larsson and A. Zetterberg, Cancer Res., 46: 1233-1239, 1986) that 25-OH inhibits the cell cycle traverse of SV-3T3 cells specifically in early G1. In contrast, treatment with serum-free medium had no effect on cell cycle progression. The effect of 25-OH on the cell cycle traverse was correlated to a substantial decrease in the activity of HMG CoA reductase, whereas there was no change in the rate of [3H]mevalonic acid incorporated into cholesterol, Coenzyme Q, and dolichol. When the cells were exposed to serum-free medium, there was no depression of activity of HMG CoA reductase, and the rate of [3H]mevalonic acid incorporated into dolichol and cholesterol was not affected in any appreciable degree. In contrast the rate of Coenzyme Q synthesis was substantially decreased as a result of serum depletion. A similar decrease in Coenzyme Q synthesis was also achieved by treating the cells with cholesterol-poor serum. This indicates that the rate of Coenzyme Q synthesis is dependent on the concentration of cholesterol in the culture medium. In order to analyze whether some of the products in the mevalonic acid biosynthetic pathway may be of importance in the control of G1 traverse and cell proliferation of SV-3T3 cells, cholesterol, Coenzyme Q, and dolichol were added as supplements to cells treated with 25-OH. It was shown that dolichol was capable of overcoming the 25-OH-induced inhibition of G1 traverse efficiently, whereas cholesterol and Coenzyme Q were considerably less effective. Considered together with the fact that the activity of HMG CoA reductase and incorporation of mevalonic acid into dolichol were unaffected following serum-free treatment, the results suggest that maintenance of a certain level of de novo synthesis of dolichol may contribute to the capability of SV-3T3 cells to proliferate in serum-free medium.

Cell Cycle↗
PubMed1987

The effect of factors released from the tumor-transformed cells on DNA synthesis, mitosis, and cellular enlargement in 3T3 fibroblasts.

Quiescent serum-starved 3T3 cells can be stimulated to initiate DNA synthesis after addition of conditioned media from spontaneously tumor-transformed 3T3 cells (3T6-cells) or from SV-40-transformed 3T3 cells (SV-3T3 cells). The conditioned media were found to stimulate both the chromosome cycle (i.e., DNA synthesis and cell division) and the growth cycle (i.e., cellular enlargement). Furthermore, addition of conditioned media to quiescent 3T3 cells increased the activity of HMG CoA reductase--an enzyme previously proposed to exercise some control on cell proliferation in 3T3 cells (Larsson and Zetterberg: J. Cell. Physiol. 129:99-102, 1986. The increased activity of HMG CoA reductase after treatment with tumor cell conditioned media was correlated to the stimulatory effects on DNA synthesis. By treating 3T3 cells stimulated to resume proliferation by addition of conditioned media with mevinolin (a competitive inhibitor of HMG CoA reductase) the activity of HMG CoA reductase as well as the DNA synthesis and cell division were efficiently inhibited. In contrast, HMG CoA activity was not coupled to the cellular enlargement. Therefore, it is proposed that one set of factors present in tumor cell conditioned media preferentially stimulates the chromosome cycle by increasing the HMG-CoA reductase activity, whereas another set of factors is responsible for growth in cell size. Both types of factors are required for balanced growth.

Animals↗
PubMed1987

Role of biosynthesis of cholesterol and isoprenoid derivatives in regulation of G1 progression and cell proliferation of 3T6 cells.

The growth of 3T6-cells was rapidly decreased, although not completely stopped, as a consequence of treatment of the cell cultures with serum-free medium. By analyzing the cell cycle traverse it was found that the decrease in growth rate was attributable to a 6-8-h delay in progression through the proximal part of G1. These effects of serum depletion on cell-cycle traverse and cell proliferation were compared with simultaneous effects on the activity of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase and the biosynthesis of cholesterol and the two isoprenoid derivatives coenzyme Q and dolichol. The activity of HMG CoA reductase was unaffected during the first 8 h of serum depletion and depressed by approximately 50% during the next 16 h. In contrast, the rate of coenzyme Q and dolichol synthesis, as related to cholesterol synthesis, was substantially decreased, and within 4 h after shift to serum-free medium both were reduced by 70-80%. As distinguished from dolichol synthesis, the synthesis of coenzyme Q was even decreased following exposures of the cell cultures to cholesterol-poor serum. This indicates that the rate of coenzyme Q synthesis is dependent on the concentration of serum cholesterol, whereas rate of dolichol synthesis is stimulated by some other serum factor(s). In addition, supplementation with dolichol to serum-depleted cells partially normalized G1 traverse and DNA synthesis, whereas cholesterol or coenzyme Q was ineffective. Taken together, the results suggest that a certain level of de novo synthesis of dolichol is required to maintain normal cell-cycle traverse and growth of 3T6 cells.

Animals↗
PubMed1987

Morbidity and mortality in diabetic and non-diabetic recipients of living related donor kidneys.

The results of kidney transplantation in juvenile-onset diabetic patients were compared to those of an age-matched control group of non-diabetic patients, all of whom were transplanted with kidneys from living related donors during the period 1977-1982, and managed by the use of conventional immunosuppression. The 5-year actuarial patient and graft survival rates did not differ significantly between the groups: 79% and 68% in diabetic patients and 88% and 72% in non-diabetic patients, respectively. The graft function was stable in both diabetic and non-diabetic patients. Early surgical complications in both groups were few. Peripheral vascular insufficiency leading to amputation occurred only in diabetic patients, while hyperparathyroidism was recorded only in non-diabetic recipients. Primary cytomegalovirus infections were more common in diabetic patients. Providing good graft function was achieved, heart complications were a minor problem in both patient groups. However, cardiovascular complications were a leading cause of death in patients whose graft failed. The initial hospital stay was, on average, one week longer in diabetic patients, but the accumulated hospital stay in the three years following transplant was twice as long (1 month per year) in the diabetic group as in the non-diabetic. Rehabilitation during the last six months of follow-up was good in both groups and about 60% of diabetic and 90% of non-diabetic patients were working full- or part-time. Thus, the prospects for survival and rehabilitation were similar in diabetic and non-diabetic patients in the 5 years following transplant, but at a higher price in diabetes.

Adolescent↗
PubMed1986

Immediate effects of serum depletion on dissociation between growth in size and cell division in proliferating 3T3 cells.

Proliferating nonconfluent 3T3 cells become committed to proceed through the cell cycle or to enter G0 during the first post-mitotic part of G1 (G1pm). The decision to proceed through G1pm is dependent on the presence of serum growth factors in the culture medium. Cells that have passed this particular growth-factor-dependent cell cycle stage are independent of serum growth factors and undergo mitosis on schedule. We report here that G1ps, S, and G2 cells cease to increase in size when serum is withdrawn. As a result the mitotic cell size after 8 hours serum starvation is reduced to approximately 60% of the normal mitotic cell. This reduced growth in cell size is due to a rapid decrease in protein synthesis and some increase in protein degradation. This dissociation between growth in size and cell-cycle progression within a single cell cycle provides a new approach to study the two processes separately.

Animals↗
PubMed1986

Effects of 25-hydroxycholesterol, cholesterol, and isoprenoid derivatives on the G1 progression in Swiss 3T3 cells.

The effect of inhibition of 3-Hydroxy-3-methylglutaryl Coenzyme A reductase (HMG CoA reductase) on cell cycle progression in proliferating 3T3 cells was studied. It was found that short transient exposures to the HMG CoA reductase inhibitor 25-hydroxycholesterol temporarily blocked the cell cycle traverse in the postmitotic half of G1 (G1pm), whereas cells in the subsequent cell cycle phases were unaffected. The kinetics of the cell cycle delay, induced by 25-hydroxycholesterol, resembled the kinetics of the delay induced by serum depletion, which also inhibited the activity of HMG CoA reductase. In contrast to the case of serum depletion, platelet derived growth factor (PDGF), which efficiently prevented the decrease of HMG CoA reductase in serum-free medium, was not capable of preventing the growth inhibitory effect following treatment by 25-hydroxycholesterol. However, cholesterol and two isoprenoids, dolichol and coenzyme Q, were effective in this respect. In addition, dolichol counteracted the cell cycle delay following short periods of serum starvation.

Cell Cycle↗
PubMed1986

Effects of VIP, PHM and substance P on blood vessels and secretory elements of the human submandibular gland.

The effects of the neuropeptides VIP, PHM and substance P (SP) on vascular smooth muscle tone, K+ secretion from exocrine elements and tissue content of cyclic AMP (cAMP) in the human submandibular gland were studied in vitro. All three peptides caused relaxation of noradrenaline contracted human submandibular arteries at nM concentrations. SP was slightly more active than VIP and PHM which had a similar potency as vasodilators. Only carbachol but not VIP, PHM or SP stimulated K+ secretion from exocrine elements of the human submandibular gland. Principally similar in vitro effects on K+ secretion were obtained on the cat submandibular gland, but in the rat not only carbachol but also SP stimulated K+ secretion. VIP and PHM increased cAMP production of exocrine elements in the human submandibular gland in nM concentrations. VIP was about 5-fold more potent than PHM with regards to cAMP production. In conclusion, VIP, PHM and SP relaxed human submandibular arteries in vitro. Both VIP and PHM stimulated cAMP production in glandular tissue but none of the three peptides induced K+ secretion from human submandibular gland tissue. This suggests that, in contrast to the situation in the rat, SP does not cause watery salivation in man, while VIP and PHM may modulate protein e.g. amylase content of the saliva.

Adult↗
PubMed1986

Left ventricular function before and after kidney transplantation. A prospective study in patients with juvenile-onset diabetes mellitus.

The aim of the present investigation was to discover whether disturbed left ventricular (LV) function limits renal replacement therapy in patients with juvenile onset diabetes mellitus. Seventeen patients given functioning kidney grafts were studied non-invasively (M-mode echocardiography, apexcardiography, phonocardiography) before renal transplant and an average of six, 13 and 44 months after transplant. The main pretransplant findings were pronounced LV hypertrophy with impaired diastolic LV function (prolonged relaxation time + signs of decreased LV distensibility) and a hyperdynamic circulation. Most of these abnormalities were significantly less severe after successful kidney transplantation. LV mass decreased by 37% 44 months after transplant (p less than 0.01) and LV diastolic and systolic volumes decreased with a subsequent increase in ejection fraction from 0.65 to 0.78 (p less than 0.01). The LV distensibility and filling pattern improved significantly while the prolonged relaxation time was unchanged. These findings imply that pretransplant disturbances in LV function are related more to factors such as hypertension, volume overload and uraemia than to diabetes per se because no pronounced improvement in the metabolic disorder resulting from diabetes can be expected, even after the most successful transplant. Disturbed LV function should not, therefore, exclude uraemic diabetics from renal replacement.

Adult↗
PubMed1986

Continuous monitoring of potassium efflux from rat parotid gland fragments by potassium selective electrodes.

The concentration of potassium ions in a superfusate of rat parotid gland fragment was continuously monitored by potassium selective electrodes to assess the rate of potassium secretion by the gland. The potassium concentration determined from the electrode readings agreed well with values obtained by atomic absorption (r = 0.99). The detection limit for changes in potassium concentration was approximated to 50 microM K+. When medium was recirculated over the gland fragments it was possible to detect even small changes in the rate of potassium efflux. Thus, increases in potassium secretion following administration of substance P (SP) down to 0.1 nM and carbacholine 10 nM was registered. When the buffer medium was passed only once over the gland fragments it was possible to reproducibly study the time course of potassium secretion. However, with this system higher doses of secretagogues were required for detection of potassium efflux, since the potassium secernated was diluted by the perifused buffer. Following SP (0.01 or 0.1 microM) or carbacholine (1 or 10 microM) a peak of potassium secretion was registered during the first 8-10 min, which was followed by a steady low rate. The metabolic state of the gland fragments, as determined by the ratio of adenine nucleotides, was similar to that found in vivo even after an experiment of several hours' duration. However, the viable part of the glandular tissue, calculated as the content of adenine nucleotides per mg protein, was decreased to approximately 30% compared to the intact gland in situ.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Autonomic mechanisms underlying capsaicin induced oral sensations and salivation in man.

The effects of capsaicin, citric acid and nicotine applied to the apex or radix of the tongue on taste sensations and salivation were studied in relation to the presence of substance P immunoreactive neurones in man. Application of capsaicin (30 micron) to the apex of the tongue or to the palatinal mucosa, but not to the radix of the tongue, caused a reproducible burning sensation and salivation from the submandibular-sublingual and parotid glands. The salivation response to capsaicin was reduced by methylscopolamine pretreatment. Similar levels of substance P immunoreactivity were present in the lingual apex and radix area (including vallate papillae) of man, while in the cat about 4 times higher levels of substance P immunoreactivity were present in the vallate papillae than in the lingual apex. Immunohistochemistry showed that in the cat many substance P immunoreactive nerves were associated with the taste buds of the vallate papillae, while in man substance P immunoreactive fibres were only seen penetrating into the epithelium of the lingual apex. In addition some subepithelial blood vessels in all regions were surrounded by substance P immunoreactive nerves in both cat and man. Citric acid application to the tongue apex caused both submandibular-sublingual and parotid salivary secretion concomitant with a burning sensation. Salivary secretion was also seen after citric acid application to the radix of the tongue. This response was associated with a sour taste. The salivation response to citric acid was not significantly reduced by methylscopolamine pretreatment. Lingual apex application of nicotine was associated with a sweet taste and a small rise in salivary secretion rate. This response was not significantly reduced by methylscopolamine. In conclusion, the sensitivity to capsaicin of the human tongue is restricted to the apex portion. This is in parallel with the occurrence of intraepithelial substance P immunoreactive nerve fibres. Capsaicin induced salivary secretion seems mainly to be mediated via parasympathetic, cholinergic reflex mechanisms. Citric acid and nicotine induced salivation responses are comparatively more resistant to methylscopolamine pretreatment.

Adolescent↗
PubMed1986

Effect of nicotine chewing gum on salivary secretion.

The effect of nicotine, placebo for nicotine or menthol-tasting chewing gums on salivation was studied in 25 healthy volunteers. The chewing of a commercial nicotine containing (2 mg) chewing gum (Nicorette) did not give a larger rate of salivation than did the chewing of a placebo chewing gum. For both types of chewing gums the rate of salivation was highest during the initial 5 min and it decreased thereafter. Menthol-tasting chewing gum gave a significantly higher amount of stimulated saliva. It is concluded that the addition of nicotine to a chewing gum does not provide an additional stimulus for salivation.

Adult↗
PubMed1986

Kinetics of G1 progression in 3T6 and SV-3T3 cells following treatment by 25-hydroxycholesterol.

The kinetics of cell cycle progression in continuously proliferating 3T3 fibroblasts and two tumor transformed derivatives (3T6 and SV 3T3 cells) following treatment by growth-factor deprivation (serum starvation) or 25-hydroxycholesterol were studied. Normal 3T3 cells were found to respond immediately (in the first cycle) to growth factor deprivation by leaving the cell cycle from G1, whereas the tumor transformed derivatives did not. However, all three cell types were forced to stop the progression through the beginning of G1 when treated by 25-hydroxycholesterol. It was ensured that the doses of 25-hydroxycholesterol used really induced substantial decrease of HMG CoA reductase activity. However, the effects of serum starvation on HMG CoA reductase activity varied considerably. In 3T3 cells HMG CoA reductase activity was substantially depressed, in 3T6 cells it was moderately depressed, and in SV-3T3 cells it was not depressed at all. This difference of HMG CoA reductase activity between 3T6 and SV-3T3 cells was related to the difference of growth activity in serum-free medium. The data indicate that a certain activity of HMG CoA reductase is required for the proliferation of normal as well as tumor transformed cells but also that impairment of the control of HMG CoA reductase, leading to increased enzyme activity, may result in uncontrolled growth in tumor transformed cells.

Animals↗